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Role of Astrocytes in Neurological Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 2772

Special Issue Editors


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Guest Editor
Center for Synaptic Neuroscience and Technologies, Istituto Italiano di Tecnologia, Genova, Italy
Interests: astroglia; brain-derived neurotrophic factor (BDNF); genetic neurodevelopmental diseases

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Guest Editor
Department of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy
Interests: astroglia; Alzheimer’s disease; neuroinflammation; brain homeostasis; calcium dynamics; transcription factors; astrocyte–neuron interaction
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Special Issue Information

Dear Colleagues,

Interest in astroglia pathophysiology has increased exponentially in recent decades. Astrocytes participate in virtually every aspect of the central nervous system’s physiology, from neuronal growth and survival to higher cognitive functions. They play a crucial role in the maintenance of nervous system homeostasis by helping neuronal maturation, regulating synaptic plasticity, and providing constant metabolic support to neurons. Alterations of these astroglial functions have been described in several neurological diseases, including both neurodegenerative and cognitive diseases. Accordingly, astrocyte-specific pathways are considered interesting targets to develop novel therapeutic strategies for these pathologies.

We believe that astrogliopathy research should get increased visibility and relevance in the scientific community. In this Special Issue, we bring together some exciting findings from young and established research groups that are active in the field of astroglia physiology and pathology.

Dr. Fabrizia Cesca
Dr. Stefano Ferroni
Guest Editors

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Keywords

  • astroglia
  • neuronal growth
  • neurological diseases

Published Papers (1 paper)

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Research

18 pages, 2247 KiB  
Article
Changes in Astroglial K+ upon Brief Periods of Energy Deprivation in the Mouse Neocortex
by Sara Eitelmann, Jonathan Stephan, Katharina Everaerts, Simone Durry, Nils Pape, Niklas J. Gerkau and Christine R. Rose
Int. J. Mol. Sci. 2022, 23(9), 4836; https://doi.org/10.3390/ijms23094836 - 27 Apr 2022
Cited by 7 | Viewed by 2244
Abstract
Malfunction of astrocytic K+ regulation contributes to the breakdown of extracellular K+ homeostasis during ischemia and spreading depolarization events. Studying astroglial K+ changes is, however, hampered by a lack of suitable techniques. Here, we combined results from fluorescence imaging, ion-selective [...] Read more.
Malfunction of astrocytic K+ regulation contributes to the breakdown of extracellular K+ homeostasis during ischemia and spreading depolarization events. Studying astroglial K+ changes is, however, hampered by a lack of suitable techniques. Here, we combined results from fluorescence imaging, ion-selective microelectrodes, and patch-clamp recordings in murine neocortical slices with the calculation of astrocytic [K+]. Brief chemical ischemia caused a reversible ATP reduction and a transient depolarization of astrocytes. Moreover, astrocytic [Na+] increased by 24 mM and extracellular [Na+] decreased. Extracellular [K+] increased, followed by an undershoot during recovery. Feeding these data into the Goldman–Hodgkin–Katz equation revealed a baseline astroglial [K+] of 146 mM, an initial K+ loss by 43 mM upon chemical ischemia, and a transient K+ overshoot of 16 mM during recovery. It also disclosed a biphasic mismatch in astrocytic Na+/K+ balance, which was initially ameliorated, but later aggravated by accompanying changes in pH and bicarbonate, respectively. Altogether, our study predicts a loss of K+ from astrocytes upon chemical ischemia followed by a net gain. The overshooting K+ uptake will promote low extracellular K+ during recovery, likely exerting a neuroprotective effect. The resulting late cation/anion imbalance requires additional efflux of cations and/or influx of anions, the latter eventually driving delayed astrocyte swelling. Full article
(This article belongs to the Special Issue Role of Astrocytes in Neurological Diseases)
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